The fibrotic lung disorders represent 15% of the non-infectious, non- malignant lung diseases; they are usually progressive and often fatal. The fibrosis results from damage caused by inflammatory cells and subsequent proliferation of mesenchymal cells, driven by mediators released by alveolar macrophage. The primary group of mediators causing the damage are oxidants. The major growth factor is platelet-derived growth factor, with the knowledge of the specific processes involved in the release of these mediators by inflammatory cells such as alveolar macrophage, strategies can be developed to modulate the expression of the genes coding for these mediators as therapy for these disorders. The granulomatous lung disorders occur in 20 to 50 per 100,000 of the USA population. The "model" disorder of this group is sarcoidosis, a disease characterized by the accumulation of activated helper/inducer T-lymphocytes at sites of disease. Evaluation of T-cells at sites of disease in these individuals demonstrates a marked bias in the populations of T-lymphocytes with similarities of the T-cell antigen receptor, including evidence for exaggerated numbers of T-lymphocytes with identical T-cell antigen receptor beta-chains. One subgroup of individuals with sarcoidosis have exaggerated numbers of alternative T-cell antigen receptor containing a gamma-delta chains. Together the studies strongly suggest that sarcoidosis is caused by an exaggerated response to a subclass of antigens or self-antigens. On this basis, strategies are being devised to understand the specific etiologies and develop appropriate therapies for this disorder.